The role of gene mutations and immune responses in sensorineural hearing loss.

Autor: Zhang X; Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China., Wu J; Department of Otolaryngology-Head and Neck Surgery, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Jiangsu Province, China., Wang M; Department of Otolaryngology, Head and Neck Surgery, The First People's Hospital of Foshan, Hearing and Balance Medical Engineering Technology Center of Guangdong, Foshan, 528000, China., Chen L; Department of Otolaryngology-Head and Neck Surgery, The Second People's Hospital of Yibin City, Sichuan Province, 644000, China., Wang P; Department of Otolaryngology-Head and Neck Surgery, Jiangdu People's Hospital Affiliated to Yangzhou University, Jiangsu Province, 225200, China., Jiang Q; Department of Neurology, Deyang Fifth Hospital, Sichuan Province, 618000, China. Electronic address: 576701372@qq.com., Yang C; Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China. Electronic address: 5247890@qq.com.
Jazyk: angličtina
Zdroj: International immunopharmacology [Int Immunopharmacol] 2024 Dec 25; Vol. 143 (Pt 3), pp. 113515. Date of Electronic Publication: 2024 Oct 31.
DOI: 10.1016/j.intimp.2024.113515
Abstrakt: Sensorineural hearing loss (SNHL) is a prevalent clinical condition primarily attributed to dysfunction within various components of the auditory pathway, spanning from the inner ear to the auditory cortex. Recent research has illuminated immune and inflammation-mediated disorders of the inner ear as critical contributors to SNHL. Disruptions in the equilibrium of inflammatory mediators, chemokines, the complement system, and inflammatory vesicles within the cochlea provoke aberrations in immune cell activity, fostering a chronic pro-inflammatory milieu that detrimentally affects the structural and functional integrity of the inner ear, culminating in hearing impairment. Specific genetic mutations, especially those affecting auditory structures, play an important role in SNHL. These mutations regulate inflammatory mediators and cellular responses, thereby altering the inflammatory dynamics within the cochlea. This review delves into the pathogenesis of sensorineural hearing loss, emphasizing the impact of genetic alterations, immune responses within the inner ear, and inflammatory mediators on auditory function. It highlights the significance of Transmembrane Serine Protease 3 (TMPRSS3) and connexin gene mutations as pivotal genetic elements in SNHL, underscoring the central role of inflammatory responses in cochlear damage. Furthermore, the paper discusses the promise of gene therapy and targeted molecular interventions, underscoring the necessity for continued exploration into the specific actions of various inflammatory agents to refine personalized therapeutic strategies.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: